BACKGROUND: IL-16 is an immunomodulatory cytokine whose expression is increased in the bronchial mucosa, bronchoalveolar lavage fluid and induced sputum of asthmatic patients. It has been suggested that IL-16 has a regulatory role in the pathophysiology of asthma. A single-nucleotide polymorphism (T(-295)C) has been described in the promoter region of the gene and it has been hypothesized that this polymorphism may be associated with altered levels of IL-16 expression, and account for the increased levels of IL-16 seen in the asthmatic airway. OBJECTIVE: To determine the association between the T(-295)C promoter polymorphism and asthma, disease severity and atopy in a large Australian Caucasian population. METHODS: We used PCR and restriction fragment length polymorphism analysis to establish the allele frequency of the T(-295)C promoter polymorphism in a random Australian Caucasian population (n=176) and to characterize the polymorphism in a large Australian Caucasian population of mild (n=273), moderate (n=230) and severe (n=77) asthmatic patients, and non-asthmatic controls (n=455). Genotype association analyses were performed using chi(2) tests. RESULTS: The polymorphic C allele was present in 19% of the asthmatic population and 21% of the non-asthmatic population. There was no association between the polymorphism and asthma (P=0.153) nor with asthma severity (P=0.417) or atopy (P=0.157) in this population. CONCLUSION: Although it has been hypothesized that the T(-295)C promoter polymorphism may be associated with increased IL-16 gene expression, it is not associated with asthma, disease severity or atopy in this Australian population.
BACKGROUND:IL-16 is an immunomodulatory cytokine whose expression is increased in the bronchial mucosa, bronchoalveolar lavage fluid and induced sputum of asthmatic patients. It has been suggested that IL-16 has a regulatory role in the pathophysiology of asthma. A single-nucleotide polymorphism (T(-295)C) has been described in the promoter region of the gene and it has been hypothesized that this polymorphism may be associated with altered levels of IL-16 expression, and account for the increased levels of IL-16 seen in the asthmatic airway. OBJECTIVE: To determine the association between the T(-295)C promoter polymorphism and asthma, disease severity and atopy in a large Australian Caucasian population. METHODS: We used PCR and restriction fragment length polymorphism analysis to establish the allele frequency of the T(-295)C promoter polymorphism in a random Australian Caucasian population (n=176) and to characterize the polymorphism in a large Australian Caucasian population of mild (n=273), moderate (n=230) and severe (n=77) asthmatic patients, and non-asthmatic controls (n=455). Genotype association analyses were performed using chi(2) tests. RESULTS: The polymorphic C allele was present in 19% of the asthmatic population and 21% of the non-asthmatic population. There was no association between the polymorphism and asthma (P=0.153) nor with asthma severity (P=0.417) or atopy (P=0.157) in this population. CONCLUSION: Although it has been hypothesized that the T(-295)C promoter polymorphism may be associated with increased IL-16 gene expression, it is not associated with asthma, disease severity or atopy in this Australian population.
Authors: Russell P Bowler; Timothy M Bahr; Grant Hughes; Sharon Lutz; Yu-Il Kim; Christopher D Coldren; Nichole Reisdorph; Katerina J Kechris Journal: OMICS Date: 2013-10-19
Authors: Wenbo Tang; Matthew Kowgier; Daan W Loth; María Soler Artigas; Bonnie R Joubert; Emily Hodge; Sina A Gharib; Albert V Smith; Ingo Ruczinski; Vilmundur Gudnason; Rasika A Mathias; Tamara B Harris; Nadia N Hansel; Lenore J Launer; Kathleen C Barnes; Joyanna G Hansen; Eva Albrecht; Melinda C Aldrich; Michael Allerhand; R Graham Barr; Guy G Brusselle; David J Couper; Ivan Curjuric; Gail Davies; Ian J Deary; Josée Dupuis; Tove Fall; Millennia Foy; Nora Franceschini; Wei Gao; Sven Gläser; Xiangjun Gu; Dana B Hancock; Joachim Heinrich; Albert Hofman; Medea Imboden; Erik Ingelsson; Alan James; Stefan Karrasch; Beate Koch; Stephen B Kritchevsky; Ashish Kumar; Lies Lahousse; Guo Li; Lars Lind; Cecilia Lindgren; Yongmei Liu; Kurt Lohman; Thomas Lumley; Wendy L McArdle; Bernd Meibohm; Andrew P Morris; Alanna C Morrison; Bill Musk; Kari E North; Lyle J Palmer; Nicole M Probst-Hensch; Bruce M Psaty; Fernando Rivadeneira; Jerome I Rotter; Holger Schulz; Lewis J Smith; Akshay Sood; John M Starr; David P Strachan; Alexander Teumer; André G Uitterlinden; Henry Völzke; Arend Voorman; Louise V Wain; Martin T Wells; Jemma B Wilk; O Dale Williams; Susan R Heckbert; Bruno H Stricker; Stephanie J London; Myriam Fornage; Martin D Tobin; George T O'Connor; Ian P Hall; Patricia A Cassano Journal: PLoS One Date: 2014-07-01 Impact factor: 3.240